Dustin L Crouch1, Johannes F Plate1, Zhongyu Li2, Katherine R Saul1. 1. Virginia Tech-Wake Forest School of Biomedical Engineering and Sciences; the Department of Biomedical Engineering and the Department of Orthopaedic Surgery, Wake Forest School of Medicine; the Neuroscience Program, Wake Forest Graduate School of Arts and Sciences, Winston-Salem; and the Department of Mechanical and Aerospace Engineering, North Carolina State University, Raleigh, North Carolina. 2. Virginia Tech-Wake Forest School of Biomedical Engineering and Sciences; the Department of Biomedical Engineering and the Department of Orthopaedic Surgery, Wake Forest School of Medicine; the Neuroscience Program, Wake Forest Graduate School of Arts and Sciences, Winston-Salem; and the Department of Mechanical and Aerospace Engineering, North Carolina State University, Raleigh, North Carolina. Electronic address: zli@wakehealth.edu.
Abstract
PURPOSE: Two mechanisms, strength imbalance or impaired longitudinal muscle growth, potentially cause osseous and postural shoulder deformity in children with brachial plexus birth palsy. Our objective was to determine which muscles, via either deformity mechanism, were mechanically capable of producing forces that could promote shoulder deformity. METHODS: In an upper limb computational musculoskeletal model, we simulated strength imbalance by allowing each muscle crossing the shoulder to produce 30% of its maximum force. To simulate impaired longitudinal muscle growth, the functional length of each muscle crossing the shoulder was reduced by 30%. We performed a sensitivity analysis to identify muscles that, through either simulated deformity mechanism, increased the posteriorly directed, compressive glenohumeral joint force consistent with osseous deformity or reduced the shoulder external rotation or abduction range of motion consistent with postural deformity. RESULTS: Most of the increase in the posterior glenohumeral joint force by the strength imbalance mechanism was caused by the subscapularis, latissimus dorsi, and infraspinatus. Posterior glenohumeral joint force increased the most owing to impaired growth of the infraspinatus, subscapularis, and long head of biceps. Through the strength imbalance mechanism, the subscapularis, anterior deltoid, and pectoralis major muscles reduced external shoulder rotation by 28°, 17°, and 10°, respectively. Shoulder motion was reduced by 40° to 56° owing to impaired growth of the anterior deltoid, subscapularis, and long head of triceps. CONCLUSIONS: The infraspinatus, subscapularis, latissimus dorsi, long head of biceps, anterior deltoid, pectoralis major, and long head of triceps were identified in this computational study as being the most capable of producing shoulder forces that may contribute to shoulder deformity following brachial plexus birth palsy. CLINICAL RELEVANCE: The muscles mechanically capable of producing deforming shoulder forces should be the focus of experimental studies investigating the musculoskeletal consequences of brachial plexus birth palsy and are potentially critical targets for treating shoulder deformity.
PURPOSE: Two mechanisms, strength imbalance or impaired longitudinal muscle growth, potentially cause osseous and postural shoulder deformity in children with brachial plexus birth palsy. Our objective was to determine which muscles, via either deformity mechanism, were mechanically capable of producing forces that could promote shoulder deformity. METHODS: In an upper limb computational musculoskeletal model, we simulated strength imbalance by allowing each muscle crossing the shoulder to produce 30% of its maximum force. To simulate impaired longitudinal muscle growth, the functional length of each muscle crossing the shoulder was reduced by 30%. We performed a sensitivity analysis to identify muscles that, through either simulated deformity mechanism, increased the posteriorly directed, compressive glenohumeral joint force consistent with osseous deformity or reduced the shoulder external rotation or abduction range of motion consistent with postural deformity. RESULTS: Most of the increase in the posterior glenohumeral joint force by the strength imbalance mechanism was caused by the subscapularis, latissimus dorsi, and infraspinatus. Posterior glenohumeral joint force increased the most owing to impaired growth of the infraspinatus, subscapularis, and long head of biceps. Through the strength imbalance mechanism, the subscapularis, anterior deltoid, and pectoralis major muscles reduced external shoulder rotation by 28°, 17°, and 10°, respectively. Shoulder motion was reduced by 40° to 56° owing to impaired growth of the anterior deltoid, subscapularis, and long head of triceps. CONCLUSIONS: The infraspinatus, subscapularis, latissimus dorsi, long head of biceps, anterior deltoid, pectoralis major, and long head of triceps were identified in this computational study as being the most capable of producing shoulder forces that may contribute to shoulder deformity following brachial plexus birth palsy. CLINICAL RELEVANCE: The muscles mechanically capable of producing deforming shoulder forces should be the focus of experimental studies investigating the musculoskeletal consequences of brachial plexus birth palsy and are potentially critical targets for treating shoulder deformity.
Authors: Raveena M Doshi; Monique Y Reid; Nikhil N Dixit; Emily B Fawcett; Jacqueline H Cole; Katherine R Saul Journal: J Orthop Res Date: 2021-09-05 Impact factor: 3.102
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